Cai ZhuLan, Xie Qingwen, Hu Tongtong, Yao Qi, Zhao Jinhua, Wu Qingqing, Tang Qizhu
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, China.
Front Cell Dev Biol. 2020 Nov 12;8:603902. doi: 10.3389/fcell.2020.603902. eCollection 2020.
Myocardial infarction (MI), the main cause of cardiovascular-related deaths worldwide, has long been a hot topic because of its threat to public health. S100A8/A9 has recently attracted an increasing amount of interest as a crucial alarmin that regulates the pathogenesis of cardiovascular disease after its release from myeloid cells. However, the role of S100A8/A9 in the etiology of MI is not well understood. Here, we elaborate on the critical roles and potential mechanisms of S100A8/A9 driving the pathogenesis of MI. First, cellular source of S100A8/A9 in infarcted heart is discussed. Then we highlight the effect of S100A8/A9 heterodimer in the early inflammatory period and the late reparative period of MI as well as myocardial ischemia/reperfusion (I/R) injury. Moreover, the predictive value of S100A8/A9 for the risk of recurrence of cardiovascular events is elucidated. Therefore, this review focuses on the molecular mechanisms of S100A8/A9 in MI pathogenesis to provide a promising biomarker and therapeutic target for MI.
心肌梗死（MI）是全球心血管相关死亡的主要原因，长期以来一直是热门话题，因为它对公众健康构成威胁。S100A8/A9作为一种关键的警报素，从髓样细胞释放后调节心血管疾病的发病机制，最近引起了越来越多的关注。然而，S100A8/A9在MI病因中的作用尚未完全明确。在此，我们阐述了S100A8/A9驱动MI发病机制的关键作用和潜在机制。首先，讨论了梗死心脏中S100A8/A9的细胞来源。然后，我们重点介绍了S100A8/A9异二聚体在MI早期炎症期和晚期修复期以及心肌缺血/再灌注（I/R）损伤中的作用。此外，还阐明了S100A8/A9对心血管事件复发风险的预测价值。因此，本综述聚焦于S100A8/A9在MI发病机制中的分子机制，为MI提供一个有前景的生物标志物和治疗靶点。
